Immune tolerance in pregnancy: Difference between revisions

* The placental [[trophoblast]] cells do not express the classical [[MHC class I]] isotypes [[HLA-A]] and [[HLA-B]], unlike most other cells in the body, and this absence is assumed to prevent destruction by maternal [[cytotoxic T cell]]s, which otherwise would recognize the fetal HLA-A and HLA-B molecules as foreign. On the other hand, they do express the atypical [[MHC class I]] isotypes [[HLA-E]] and [[HLA-G]], which is assumed to prevent destruction by maternal [[NK cells]], which otherwise destroy cells that do not express any [[MHC class I]].<ref name=creasy>Page 31 to 32 in: Maternal-Fetal Medicine : Principles and Practice. Editor: Robert K. Creasy, Robert Resnik, Jay D. Iams. {{ISBN|978-0-7216-0004-8}} Published: September 2003</ref> However, trophoblast cells do express the rather typical [[HLA-C]].<ref name=creasy/>

*It forms a [[syncytium]] without any extracellular spaces between cells in order to limit the exchange of migratory immune cells between the developing embryo and the body of the mother (something an [[epithelium]] will not do sufficiently, as certain blood cells are specialized to be able to insert themselves between adjacent epithelial cells). The fusion of the cells is apparently caused by [[viral fusion proteins]] from [[Endogenous retrovirus#Endosymbiotic ERVs in mammals|endosymbiotic endogenous retrovirus (ERV)]].<ref>{{cite journal |vauthors=Mi S, Lee X, Li X, etal |title=Syncytin is a captive retroviral envelope protein involved in human placental morphogenesis |journal=Nature |volume=403 |issue=6771 |pages=785–9 |date=Feb 2000 |pmid=10693809 |doi=10.1038/35001608 }}

 

Still, the placenta does allow maternal [[IgG antibodies]] to pass to the fetus to protect it against infections. However, these antibodies do not target fetal cells, unless any fetal material has escaped across the placenta where it can come in contact with maternal [[B cell]]s and make those B cells start to produce antibodies against fetal targets. The mother does produce antibodies against foreign [[ABO blood types]], where the fetal blood cells are possible targets, but these preformed antibodies are usually of the [[IgM antibodies|IgM]] type,<ref name=barbreau>[http://www.freshpatents.com/Magnetic-immunodiagnostic-method-for-the-demonstration-of-antibody-antigen-complexes-especially-of-blood-groups-dt20091029ptan20090269776.php Magnetic immunodiagnostic method for the demonstration of antibody/antigen complexes especially of blood groups] {{webarchive|url=https://web.archive.org/web/20120229032947/http://www.freshpatents.com/Magnetic-immunodiagnostic-method-for-the-demonstration-of-antibody-antigen-complexes-especially-of-blood-groups-dt20091029ptan20090269776.php |date=2012-02-29 }} Yves Barbreau, Olivier Boulet, Arnaud Boulet, Alexis Delanoe, Laurence Fauconnier, Fabien Herbert, Jean-Marc Pelosin, Laurent Soufflet. October 2009</ref> and therefore usually do not cross the placenta. Still, rarely, ABO incompatibility can give rise to IgG antibodies that cross the placenta, and are caused by sensitization of mothers (usually of blood type 0) to antigens in foods or bacteria.<ref>[http://www.merckmanuals.com/professional/sec19/ch273/ch273b.html Merck manuals > Perinatal Anemia] Last full review/revision January 2010 by David A. Paul</ref>

 

*'''[[Rh disease]]''' is caused by the mother producing [[Antibody|antibodies]] (including [[IgG antibodies]]) against the [[Rhesus blood group system|Rhesus D]] [[antigen]] on her baby's [[red blood cell]]s. It occurs if the mother is Rh negative and the baby is Rh positive, and a small amount of Rh positive blood from any previous pregnancy has entered the mother's circulation to make her produce IgG antibodies against the D antigen (Anti-D). Maternal IgG is able to pass through the [[placenta]] into the [[fetus]] and if the level of it is sufficient, it will cause destruction of D positive fetal red blood cells leading to development of the anti-Rh type of [[hemolytic disease of the newborn|hemolytic disease of the fetus and newborn]] (HDFN). Generally HDFN becomes worse with each additional Rh incompatible pregnancy.

 

Pregnancies resulting from [[egg donation]], where the carrier is less genetically similar to the fetus than a biological mother, are associated with a higher incidence of [[pregnancy-induced hypertension]] and [[placental pathology]].<ref name=van-der-Hoorn2010/> The local and systemic immunologic changes are also more pronounced than in normal pregnancies, so it has been suggested that the higher frequency of some conditions in egg donation may be caused by reduced immune tolerance from the mother.<ref name=van-der-Hoorn2010>{{Cite journal | doi = 10.1093/humupd/dmq017| last1 = Van Der Hoorn | first1 = M. L. P. | last2 = Lashley | first2 = E. E. L. O. | last3 = Bianchi | first3 = D. W. | last4 = Claas | first4 = F. H. J. | last5 = Schonkeren | first5 = C. M. C. | last6 = Scherjon | first6 = S. A. | title = Clinical and immunologic aspects of egg donation pregnancies: a systematic review | journal = Human Reproduction Update | volume = 16 | issue = 6 | pages = 704–12 | date = Nov-Dec 2010 | pmid = 20543201}}</ref>